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Circulation Research. 2000;86:1004-1007

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(Circulation Research. 2000;86:1004.)
© 2000 American Heart Association, Inc.


Clinical Research

Activation of Mitogen-Activated Protein Kinases in Human Heart During Cardiopulmonary Bypass

Daniel Talmor, Azai Applebaum, Assaf Rudich, Yoram Shapira, Amir Tirosh

From the Division of Anesthesiology (D.T., Y.S.), Department of Cardiothoracic Surgery (A.A.), The S. Daniel Abraham Center for Health and Nutrition (A.R.), and the Department of Clinical Biochemistry (A.T.), Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Correspondence to Amir Tirosh, MD, Department of Clinical Biochemistry, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel, IL-84105. E-mail amirt{at}bgumail.bgu.ac.il

Abstract—Mitogen-activated protein kinases (MAPKs) have been shown to be activated in both in vitro and in vivo models of cardiac tissue in response to ischemia/reperfusion injury. We investigated whether MAPKs are activated in human heart during coronary artery bypass grafting (CABG) surgery. During elective CABG surgery of 8 patients, 3 right atrial appendage biopsies were obtained at baseline, at the end of cross-clamping, and after coronary reperfusion. The expression of the p38-MAPK, c-Jun N-terminal kinase (JNK), and extracellular signal–regulated kinases (ERK1/2) MAPKs was not altered during CABG. The phosphorylation and activation of both ERK1/2 and p38-MAPK were increased {approx}2-fold by ischemia and even more (8- and 4-fold, respectively) by reperfusion. Although the ischemic period did not result in a significant activation of JNK, an {approx}6-fold increase in JNK activity could be observed after reperfusion. In conclusion, distinct activation patterns of ERK1/2, p38, and JNK MAPKs can be observed in human heart during CABG.


Key Words: myocardium • ischemia/reperfusion • stress-activated protein kinases




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